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Hyperglycemia and cardiomyocytes

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https://www.readbyqxmd.com/read/30280191/overexpression-of-small-ubiquitin%C3%A2-like-modifier-2-ameliorates-high-glucose%C3%A2-induced-reductions-in-cardiomyocyte-proliferation-via-the-transforming-growth-factor%C3%A2-%C3%AE-smad-pathway
#1
Chen Zhao, Qile Shen
Hyperglycemia may induce diabetic cardiomyopathy (DC). In the current study, the mechanism underlying the alleviation of high glucose (HG)‑induced impairments in the proliferation of H9c2 embryo cardiomyocyte proliferation by small ubiquitin‑like modifier 2 (SUMO2) overexpression was investigated. H9c2 cell morphology was identified as classical long shuttle type by optical microscopy. The viability of HG‑injured H9c2 cells was evaluated by a Cell Counting Kit‑8 assay and the results indicated that viability was inhibited in a dose‑dependent (5...
October 1, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/30132875/heat-shock-protein-70-a-promising-therapeutic-target-for-myocardial-ischemia-reperfusion-injury
#2
REVIEW
Yan-Jun Song, Chong-Bin Zhong, Xian-Bao Wang
Acute myocardial infarction is a major cause of death worldwide. The most important therapy for limiting ischemic injury and infarct size is timely and efficient myocardial reperfusion treatment, which may instead induce cardiomyocyte necrosis due to myocardial ischemia-reperfusion (I/R) injury. Heat shock protein 70 (HSP70), a stress-inducible protein, is overexpressed during myocardial I/R. The induced HSP70 is shown to regulate several intracellular proteins (e.g., transcription factors, enzymes, and apoptosis-related proteins) and signaling pathways (e...
August 21, 2018: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/30091070/a-brief-overview-from-the-physiological-and-detrimental-roles-of-zinc-homeostasis-via-zinc-transporters-in-the-heart
#3
Belma Turan
Zinc (mostly as free/labile Zn2+ ) is an essential structural constituent of many proteins, including enzymes in cellular signaling pathways via functioning as an important signaling molecule in mammalian cells. In cardiomyocytes at resting condition, intracellular labile Zn2+ concentration ([Zn2+ ]i ) is in the nanomolar range, whereas it can increase dramatically under pathological conditions, including hyperglycemia, but the mechanisms that affect its subcellular redistribution is not clear. Therefore, overall, very little is known about the precise mechanisms controlling the intracellular distribution of labile Zn2+ , particularly via Zn2+ transporters during cardiac function under both physiological and pathophysiological conditions...
August 8, 2018: Biological Trace Element Research
https://www.readbyqxmd.com/read/30048968/high-fat-diet-upregulates-fatty-acid-oxidation-and-ketogenesis-via-intervention-of-ppar-%C3%AE
#4
Kunal Sikder, Sanket Kumar Shukla, Neel Patel, Harpreet Singh, Khadija Rafiq
BACKGROUND/AIMS: Systemic hyperlipidemia and intracellular lipid accumulation induced by chronic high fat diet (HFD) leads to enhanced fatty acid oxidation (FAO) and ketogenesis. The present study was aimed to determine whether activation of peroxisome proliferator-activated receptor-γ (PPAR-γ) by surplus free fatty acids (FA) in hyperlipidemic condition, has a positive feedback regulation over FAO and ketogenic enzymes controlling lipotoxicity and cardiac apoptosis. METHODS: 8 weeks old C57BL/6 wild type (WT) or PPAR-γ-/- mice were challenged with 16 weeks 60% HFD to induce obesity mediated type 2 diabetes mellitus (T2DM) and diabetic cardiomyopathy...
2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/30004258/characterization-of-a-mouse-model-of-obesity-related-fibrotic-cardiomyopathy-that-recapitulates-features-of-human-heart-failure-with-preserved-ejection-fraction
#5
Linda Alex, Ilaria Russo, Volodymir Holoborodko, Nikolaos G Frangogiannis
Heart failure with preserved ejection fraction (HFpEF) is caused, or exacerbated by, a wide range of extracardiac conditions. Diabetes, obesity, and metabolic dysfunction are associated with a unique HFpEF phenotype, characterized by inflammation, cardiac fibrosis, and microvascular dysfunction. Development of new therapies for HFpEF is hampered by the absence of reliable animal models. The leptin-resistant db/ db mouse has been extensively studied as a model of diabetes-associated cardiomyopathy; however, data on the functional and morphological alterations in db/ db hearts are conflicting...
October 1, 2018: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/30002788/cytoprotective-roles-of-a-novel-compound-mhy-1684-against-hyperglycemia-induced-oxidative-stress-and-mitochondrial-dysfunction-in-human-cardiac-progenitor-cells
#6
Woong Bi Jang, Ji Hye Park, Seung Taek Ji, Na Kyung Lee, Da Yeon Kim, Yeon Ju Kim, Seok Yun Jung, Songhwa Kang, Shreekrishna Lamichane, Babita Dahal Lamichane, Jongseong Ha, Jisoo Yun, Hyung Ryong Moon, Sang Hong Baek, Hae Young Chung, Sang-Mo Kwon
Diabetic cardiomyopathy (DCM) is tightly linked to heart disorders and dysfunction or death of the cardiomyocytes including resident cardiac progenitor cells (CPCs) in diabetic patients. In order to restore loss of function of resident or transplanted CPCs, much research has focused on novel therapeutic strategies including the discovery of novel function-modulating factors such as reactive oxygen species (ROS) scavengers. Here, we developed and defined a novel antioxidant, MHY-1684, for enhancing the angiogenic potential of CPCs against ROS-related DCM...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29903013/inhibition-of-calcium-calmodulin-dependent-kinase-ii-restores-contraction-and-relaxation-in-isolated-cardiac-muscle-from-type-2-diabetic-rats
#7
Lorna J Daniels, Rachel S Wallace, Olivia M Nicholson, Genevieve A Wilson, Fiona J McDonald, Peter P Jones, J Chris Baldi, Regis R Lamberts, Jeffrey R Erickson
BACKGROUND: Calcium/calmodulin-dependent kinase II-delta (CaMKIIδ) activity is enhanced during hyperglycemia and has been shown to alter intracellular calcium handling in cardiomyocytes, ultimately leading to reduced cardiac performance. However, the effects of CaMKIIδ on cardiac contractility during type 2 diabetes are undefined. METHODS: We examined the expression and activation of CaMKIIδ in right atrial appendages from non-diabetic and type 2 diabetic patients (n = 7 patients per group) with preserved ejection fraction, and also in right ventricular tissue from Zucker Diabetic Fatty rats (ZDF) (n = 5-10 animals per group) during early diabetic cardiac dysfunction, using immunoblot...
June 14, 2018: Cardiovascular Diabetology
https://www.readbyqxmd.com/read/29782963/bet-inhibition-by-jq1-alleviates-streptozotocin-induced-diabetic-cardiomyopathy
#8
Miao Guo, Hong-Xia Wang, Wen-Jun Chen
Diabetic cardiomyopathy is a cascade of complex events leading to eventual heart failure in diabetes. JQ1, one of Bromodomain and extra-terminal domain (BET) protein inhibitors, has exerted therapeutic effects on cancer proliferation, inflammation and cardiovascular disease. Recently, JQ1 was reported to protect mice from bleomycin-induced lung fibrosis and reverse the fibrotic response in carbon tetrachloride-induced liver fibrosis. However, its role in diabetic cardiomyopathy remains to be clarified. Our results indicated that JQ1 treatment suppressed cardiac fibrosis and improved cardiac function in a STZ-induced diabetic mouse model...
August 1, 2018: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/29726706/hibiscus-sabdariffa-roselle-polyphenol-rich-extract-averts-cardiac-functional-and-structural-abnormalities-in-type-1-diabetic-rats
#9
Nur Liyana Mohammed Yusof, Satirah Zainalabidin, Norsyahida Mohd Fauzi, Siti Balkis Budin
Diabetes mellitus is often associated with cardiac functional and structural alteration, an initial event leading to cardiovascular complications. Roselle (Hibiscus sabdariffa) has been widely proven as an antioxidant and recently has incited research interest for its potential in treating cardiovascular disease. Therefore, this study aimed to determine the cardioprotective effects of H. sabdariffa (roselle) polyphenol-rich extract (HPE) in type-1-induced diabetic rats. Twenty-four male Sprague-Dawley rats were randomized into 4 groups (n = 6/group): nondiabetic, diabetic alone (DM), diabetic supplemented with HPE (DM+HPE), and diabetic supplemented with metformin...
May 4, 2018: Applied Physiology, Nutrition, and Metabolism, Physiologie Appliquée, Nutrition et Métabolisme
https://www.readbyqxmd.com/read/29719509/mangiferin-enhanced-autophagy-via-inhibiting-mtorc1-pathway-to-prevent-high-glucose-induced-cardiomyocyte-injury
#10
Jun Hou, Dezhi Zheng, Wenjing Xiao, Dandan Li, Jie Ma, Yonghe Hu
Mangiferin functions as a perfect anti-oxidative compound in the diabetic heart, however, the exact mechanism remains to be elucidated. Here, we show the cardioprotective effect of mangiferin under high glucose-induced cardiotoxic condition mainly contributed to enhanced autophagy via suppressing mTORC1 downstream signal transduction. Primary neonatal rat cardiomyocytes were cultured to detect myocytes injury, autophagy, and related signal transduction under different doses of glucose and mangiferin treatment...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29459772/monoamine-oxidase-dependent-endoplasmic-reticulum-mitochondria-dysfunction-and-mast-cell-degranulation-lead-to-adverse-cardiac-remodeling-in-diabetes
#11
Soni Deshwal, Marleen Forkink, Chou-Hui Hu, Guido Buonincontri, Salvatore Antonucci, Moises Di Sante, Michael P Murphy, Nazareno Paolocci, Daria Mochly-Rosen, Thomas Krieg, Fabio Di Lisa, Nina Kaludercic
Monoamine oxidase (MAO) inhibitors ameliorate contractile function in diabetic animals, but the mechanisms remain unknown. Equally elusive is the interplay between the cardiomyocyte alterations induced by hyperglycemia and the accompanying inflammation. Here we show that exposure of primary cardiomyocytes to high glucose and pro-inflammatory stimuli leads to MAO-dependent increase in reactive oxygen species that causes permeability transition pore opening and mitochondrial dysfunction. These events occur upstream of endoplasmic reticulum (ER) stress and are abolished by the MAO inhibitor pargyline, highlighting the role of these flavoenzymes in the ER/mitochondria cross-talk...
September 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29450407/changes-in-the-cardiac-ghsr1a-ghrelin-system-correlate-with-myocardial-dysfunction-in-diabetic-cardiomyopathy-in-mice
#12
Rebecca Sullivan, Rebecca McGirr, Shirley Hu, Alice Tan, Derek Wu, Carlie Charron, Tyler Lalonde, Edith Arany, Subrata Chakrabarti, Leonard Luyt, Savita Dhanvantari
Ghrelin and its receptor, the growth hormone secretagogue receptor 1a (GHSR1a), are present in cardiac tissue. Activation of GHSR1a by ghrelin promotes cardiomyocyte contractility and survival, and changes in myocardial GHSR1a and circulating ghrelin track with end-stage heart failure, leading to the hypothesis that GHSR1a is a biomarker for heart failure. We hypothesized that GHSR1a could also be a biomarker for diabetic cardiomyopathy (DCM). We used two models of streptozotocin (STZ)-induced DCM: group 1, adult mice treated with 35 mg/kg STZ for 3 days; and group 2, neonatal mice treated with 70 mg/kg STZ at days 2 and 5 after birth...
February 1, 2018: Journal of the Endocrine Society
https://www.readbyqxmd.com/read/29443547/modeling-heart-failure-risk-in-diabetes-and-kidney-disease-limitations-and-potential-applications-of-transverse-aortic-constriction-in-high-fat-fed-mice
#13
Wei Sheng Tan, Thomas P Mullins, Melanie Flint, Sarah L Walton, Helle Bielefeldt-Ohmann, David A Carter, Meera R Gandhi, Hayley R McDonald, Joan Li, Karen M Moritz, Melissa E Reichelt, Linda A Gallo
There is an increased incidence of heart failure in individuals with diabetes mellitus (DM). The coexistence of kidney disease in DM exacerbates the cardiovascular prognosis. Researchers have attempted to combine the critical features of heart failure, using transverse aortic constriction, with DM in mice, but variable findings have been reported. Furthermore, kidney outcomes have not been assessed in this setting; thus its utility as a model of heart failure in DM and kidney disease is unknown. We generated a mouse model of obesity, hyperglycemia, and mild kidney pathology by feeding male C57BL/6J mice a high-fat diet (HFD)...
June 1, 2018: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
https://www.readbyqxmd.com/read/29432575/multiple-common-comorbidities-produce-left-ventricular-diastolic-dysfunction-associated-with-coronary-microvascular-dysfunction-oxidative-stress-and-myocardial-stiffening
#14
Oana Sorop, Ilkka Heinonen, Matthijs van Kranenburg, Jens van de Wouw, Vincent J de Beer, Isabel T N Nguyen, Yanti Octavia, Richard W B van Duin, Kelly Stam, Robert-Jan van Geuns, Piotr A Wielopolski, Gabriel P Krestin, Anton H van den Meiracker, Robin Verjans, Marc van Bilsen, A H Jan Danser, Walter J Paulus, Caroline Cheng, Wolfgang A Linke, Jaap A Joles, Marianne C Verhaar, Jolanda van der Velden, Daphne Merkus, Dirk J Duncker
Aims: More than 50% of patients with heart failure have preserved ejection fraction characterized by diastolic dysfunction. The prevalance of diastolic dysfunction is higher in females and associates with multiple comorbidities such as hypertension (HT), obesity, hypercholesterolemia (HC), and diabetes mellitus (DM). Although its pathophysiology remains incompletely understood, it has been proposed that these comorbidities induce systemic inflammation, coronary microvascular dysfunction, and oxidative stress, leading to myocardial fibrosis, myocyte stiffening and, ultimately, diastolic dysfunction...
June 1, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29392616/kaempferol-attenuates-hyperglycemia-induced-cardiac-injuries-by-inhibiting-inflammatory-responses-and-oxidative-stress
#15
Xuemei Chen, Jianchang Qian, Lintao Wang, Jieli Li, Yunjie Zhao, Jibo Han, Zia Khan, Xiaojun Chen, Jingying Wang, Guang Liang
PURPOSE: Suppression of inflammation and oxidative stress is an attractive strategy to against diabetic cardiomyopathy (DCM). Kaempferol (KPF) exerts both anti-inflammatory and antioxidant pharmacological properties. However, little is known about the effect of KPF on protecting myocardial injury in diabetes. The present study aimed to investigate the effect of KPF on DCM and underlying mechanism. METHODS: Anti-inflammation and anti-oxidative stress activities of KPF were evaluated in H9c2 cells or primary cardiomyocytes by real-time quantitate PCR, immunoblotting, immunofluorescence, ELISA, and FACS...
April 2018: Endocrine
https://www.readbyqxmd.com/read/29392082/apelin-ameliorates-high-glucose-induced-downregulation-of-connexin-43-via-ampk-dependent-pathway-in-neonatal-rat-cardiomyocytes
#16
Xiaoting Li, Lu Yu, Jing Gao, Xukun Bi, Juhong Zhang, Shiming Xu, Meihui Wang, Mengmeng Chen, Fuyu Qiu, Guosheng Fu
Diabetes Mellitus is a common disorder, with increasing risk of cardiac arrhythmias. Studies have shown that altered connexin expression and gap junction remodeling under hyperglycemia contribute to the high prevalence of cardiac arrhythmias and even sudden death. Connexin 43 (Cx43), a major protein that assembles to form cardiac gap junctions, has been found to be downregulated under high glucose conditions, along with inhibition of gap junctional intercellular communication (GJIC). While, apelin, a beneficial adipokine, increases Cx43 protein expression in mouse and human embryonic stem cells during cardiac differentiation...
February 2018: Aging and Disease
https://www.readbyqxmd.com/read/29325553/sitagliptin-improved-glucose-assimilation-in-detriment-of-fatty-acid-utilization-in-experimental-type-ii-diabetes-role-of-glp-1-isoforms-in-glut4-receptor-trafficking
#17
E Ramírez, B Picatoste, A González-Bris, M Oteo, F Cruz, A Caro-Vadillo, J Egido, J Tuñón, M A Morcillo, Ó Lorenzo
BACKGROUND: The distribution of glucose and fatty-acid transporters in the heart is crucial for energy consecution and myocardial function. In this sense, the glucagon-like peptide-1 (GLP-1) enhancer, sitagliptin, improves glucose homeostasis but it could also trigger direct cardioprotective actions, including regulation of energy substrate utilization. METHODS: Type-II diabetic GK (Goto-Kakizaki), sitagliptin-treated GK (10 mg/kg/day) and wistar rats (n = 10, each) underwent echocardiographic evaluation, and positron emission tomography scanning for [18 F]-2-fluoro-2-deoxy-D-glucose (18 FDG)...
January 11, 2018: Cardiovascular Diabetology
https://www.readbyqxmd.com/read/29231167/glucose-inhibits-cardiac-muscle-maturation-through-nucleotide-biosynthesis
#18
Haruko Nakano, Itsunari Minami, Daniel Braas, Herman Pappoe, Xiuju Wu, Addelynn Sagadevan, Laurent Vergnes, Kai Fu, Marco Morselli, Christopher Dunham, Xueqin Ding, Adam Z Stieg, James K Gimzewski, Matteo Pellegrini, Peter M Clark, Karen Reue, Aldons J Lusis, Bernard Ribalet, Siavash K Kurdistani, Heather Christofk, Norio Nakatsuji, Atsushi Nakano
The heart switches its energy substrate from glucose to fatty acids at birth, and maternal hyperglycemia is associated with congenital heart disease. However, little is known about how blood glucose impacts heart formation. Using a chemically defined human pluripotent stem-cell-derived cardiomyocyte differentiation system, we found that high glucose inhibits the maturation of cardiomyocytes at genetic, structural, metabolic, electrophysiological, and biomechanical levels by promoting nucleotide biosynthesis through the pentose phosphate pathway...
December 12, 2017: ELife
https://www.readbyqxmd.com/read/29221204/11%C3%AE-hsd1-inhibition-ameliorates-diabetes-induced-cardiomyocyte-hypertrophy-and-cardiac-fibrosis-through-modulation-of-egfr-activity
#19
Chunpeng Zou, Weixin Li, Yong Pan, Zia A Khan, Jieli Li, Xixi Wu, Yi Wang, Liancheng Deng, Guang Liang, Yunjie Zhao
11β-HSD1 has been recognized as a potential therapeutic target for type 2 diabetes. Recent studies have shown that hyperglycemia leads to activation of 11β-HSD1, increasing the intracellular glucocorticoid levels. Excess glucocorticoids may lead to the clinical manifestations of cardiac injury. Therefore, the aim of this study is to investigate whether 11β-HSD1 activation contributes to the development of diabetic cardiomyopathy. To investigate the role of 11β-HSD1, we administered a selective 11β-HSD1 inhibitor in type 1 and type 2 murine models of diabetes and in cultured cardiomyocytes...
November 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/29192360/hyperglycemia-induced-cardiac-contractile-dysfunction-in-the-diabetic-heart
#20
REVIEW
Raphael M Singh, Tahreem Waqar, Frank C Howarth, Ernest Adeghate, Keshore Bidasee, Jaipaul Singh
The development of a diabetic cardiomyopathy is a multifactorial process, and evidence is accumulating that defects in intracellular free calcium concentration [Ca2+ ]i or its homeostasis are related to impaired mechanical performance of the diabetic heart leading to a reduction in contractile dysfunction. Defects in ryanodine receptor, reduced activity of the sarcoplasmic reticulum calcium pump (SERCA) and, along with reduced activity of the sodium-calcium exchanger (NCX) and alterations in myofilament, collectively cause a calcium imbalance within the diabetic cardiomyocytes...
January 2018: Heart Failure Reviews
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